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There is a lack of validated predictors on which to decide the timing of discharge in patients already hospitalized for upper nonvariceal bleeding.Identify factors that appear to protect nonvariceal bleeders from the development of negative outcome (rebleeding, surgery, death).Secondary analysis of two prospective multicenter studies. Multivariate analyses for each investigated outcome were performed; a single model was developed including all factors that were statistically significant in each sub-model. A final score was developed to predict favourable outcomes. Prognostic accuracy was tested with ROC curve analysis.Out of 2398 patients, 211 (8.8%) developed one or more adverse outcomes: 87 (3.63%) had rebleeding, 46 (1.92%) needed surgery and 107 (4.46%) died. Predictors of favourable prognosis were: ASA score 1 or 2, absence of neoplasia, outpatient bleeding, use of low-dose aspirin, no need for transfusions, clean-based ulcer, age70 years, no haemodynamic instability successful endoscopic diagnosis/therapy, no Dieulafoy's lesion at endoscopy, no hematemesis on presentation and no need for endoscopic treatment. Overall prognostic accuracy of the model was 83%. The final score accurately identified 20-30% of patients that eventually do not develop any negative outcome.The "good luck score" may be a useful tool in deciding when to discharge a patient already hospitalized for acute non-variceal bleeding.

From an Italian Registry of patients with upper gastrointestinal hemorrhage (UGIH), we assessed the clinical outcomes and explored the roles of clinical, endoscopic, and therapeutic factors on 30-day mortality in a real life setting.Prospective analysis of consecutive patients endoscoped for UGIH at 23 community and tertiary care institutions from 2003 to 2004. Covariates and outcomes were defined a priori and 30-day follow-up obtained. Logistic regression analysis identified predictors of mortality.One thousand and twenty patients were included. A total of 46 patients died for an overall 4.5% mortality rate. In all, 85% of deaths were associated with one or more major comorbidity. Sixteen of 46 patients (35%) died within the first 24 h of the onset of bleeding. Of these, eight had been categorized as ASA class 1 or 2 and none of them was operated upon, despite a failure of endoscopic intention to treatment in four. Regression analysis showed advanced age, presence of severe comorbidity, low hemoglobin levels at presentation, and worsening health status as the only independent predictors of 30-day mortality (P0.001). The acute use of a PPI exerted a protective effect (OR 0.23, 95% CI 0.09-0.73). Recurrent bleeding was low (3.2%). Rebleeders accounted for only 11% of the total patients deceased (OR 3.27, 95% CI 1.5-11.2).These results indicate that 30-day mortality for nonvariceal bleeding is low. Deaths occurred predominantly in elderly patients with severe comorbidities or those with failure of endoscopic intention to treatment.

Follow-up after endoscopic polypectomy should be led by the number, size, and histopatologic characteristics of the polyps at the baseline colonoscopy. In a patient with large sessile polyps and incomplete excision, a follow-up colonoscopy at 2-6 months is suggested. After curative resection of invasive carcinoma or malignant polyps, intense colonoscopy follow-up at 1 year is mandatory. Patients with high-grade dysplasia adenoma, villous histology, polyps larger than 10 mm, or more than three polyps have an intermediate risk of advanced neoplasia, and surveillance at 3 years is recommended. Patients with 1-2 small tubular adenomas should undergo surveillance colonoscopy at 5-10 years; in patients with negative or sporadic hyperplastic polyps at baseline colonoscopy, surveillance is now suggested after 10 years.

To have a better understanding of the role of endoscopy in familial adenomatous polyposis, it is necessary to clarify some concepts in colon cancer development. Colon cancer (CRC) arises from a dysplastic precursor lesion called adenomatous polyp (or adenoma). Approximately 30–40% of people over 50 years of age will develop an adenoma, but not all adenomas will progress to CRC. In the general population some individuals tend to develop one or only a few adenomas and endoscopic polypectomy is often sufficient for removing them, thereby markedly reducing the subsequent development to CRC. Adenomas arise when both copies of the APC gene are lost. Indeed, the APC gene is considered the “gatekeeper” of the colon, protecting against the development of adenomas. The loss of APC gene function permits adenoma formation and sets the stage for subsequent molecular alterations of genes such as kras and p53, which promote further progression to CRC (Fig. 1). Some people develop multiple polyps of the colon at a younger age due to inheritance of a germline mutation of a gene that predisposes to CRC. Since these patients are at increased risk of CRC (and other types of cancer), it is important to recognize these syndromes earlier (Table 1). Therefore, endoscopic procedures play a crucial role in the diagnosis, staging and follow-up of these conditions.